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Query: UMLS:C0019158 (hepatitis)
 30,205 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

two patients with polyarteritis nodosa who presented with vague constitutional systems and hepatitis-B antigenemia are reported. Angiography was used as the primary diagnostic procedure and confirmed the diagnosis in each case. Angiography is a relatively simple and direct means for establishing the diagnosis of polyarteritis nodosa. In these patients, the typical finding of aneurysm formation in multiple organs was observed. Arterial narrowing was also widespread. Multiple renal infarcts are shown in one case, and bronchial arteriography revealed aneurysms and narrowing in bronchial and intercostal arteries in one patient who had a recent pulmonary infarction and a normal pulmonary arteriogram. The relationship of the hepatitis-B antigen and polyarteritis is also emphasized.
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PMID:Polyarteritis nodosa and hepatitis-B surface antigen: role of angiography in diagnosis. 1 66

In 7 unselected necropsy cases of clinically diagnosed periarteritis nodosa, the detection of hepatitis B surface antigen (HBsAg) and hepatitis B core antigen (HBcAg) in the cytoplasm and nuclei of hepatocytes indicated an ongoing infection with hepititis B virus (HBV). In all these cases histologic changes found in the liver varied from "minimal" to chronic aggressive hepatitis. In all the cases, deposits of HBsAg, immunoglobulins, beta1C-globulin and C1q were detected in vascular lesions. That these deposits could represent HBsAg-anti-HBs immune complexes was supported by demonstrating their strong binding of guinea pig complement and by the successful elution of all HBsAg and part of the immunoglobulin from these deposits by treatment with buffers known to dissociate antigen-antibody bonds but not with phosphate-buffered saline, pH 7.6 (PBS). Glomerulonephritis associated with these immune complexes was found in 6 cases. The presence of larger masses of HBsAg immune complexes, chiefly in recent insudative and fibrinoid vascular lesions, their lesser amounts in lesions undergoing involution, and their absence from healed lesions strongly suggest that these complexes play a primary role in the pathogenesis of acute vascular damage in periarteritis nodosa.
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PMID:Immune complexes of hepatitis B surface antigen in the pathogenesis of periarteritis nodosa. A study of seven necropsy cases. 2 42

There are two well-characterized antigen-antibody systems which relate specificially to viral hepatitis B. Tests for HBsAg and anti-HBs are readily available and of great benefit to the diagnosis, prevention and understanding of hepatitis B. Tests for HBcAg and anti-HBc are still research techniques which requires further development before they can be used at the level of everyday medical practice. HBsAg in an individual indicates that he harbors the virus of hepatitis B; it may be present in the absence of liver disease or be found in association with both acute and chronic type B hepatitis. The presence of HBsAg also suggests that HBV may be causally related to some cases of periarteritis nodosa, chronic glomerulonephritis, and hepatoma. Although HBV is readily transmitted in blood, the major portion of post-transfusion hepatitis now appears to be serologically unrelated to either the hepatitis B virus ("serum") or the hepatitis A virus ("infectious"); the etiology of these cases is currently undetermined. There is increasing evidence that HBV may be transmitted by modes other than blood, but the exact mechanisms of such transmission is not established. The combined transmission of HBV by blood and other routes has resulted in a large number of persistent carriers of HBsAg in the world. There is no current method to alter this carrier state. The hepatitis risk of such persistent carriers to their personal and professional contacts is under investigation.
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PMID:The clinical significance of hepatitis B virus antigens and antibodies. 4 64

Testing for e antigen and antibody (anti-e) was performed by immunodiffusion and counterelectrophoresis in patients with polyarteritis nodosa fulminant hepatitis, and chronic active hepatitis (CAH), in 59 asymptomatic carriers of hepatitis B surface antigen (HBsAg) who underwent liver biopsy, and in 150 carriers followed with sequential SGPT determinations. Counterelectrophoresis was more sensitive that immunodiffusion. Neither e antigen nor anti-e was found in the absence of HBsAg. Among HCsAg-positive patients with polyarteritis nodosa and CAH, e antigen was found in 16 of 18 and 13 of 22, respectively. It was not found in any of 43 patients with fulminant hepatitis, of whom 24 were HBsAg-positive. The e antigen was detected in none of 13 biopsied carriers with normal histology, 4 of 28 with nonspecific changes of 11 of 18 with CAH or chronic persistent hepatitis. Conversely, anti-e was present in 9 of 13 with normal biopsy, 7 of 28 with nonspecific changes, and none of 18 with CAH or chronic persistent hepatitis. The e antigen was found more commonly in nonbiopsied carriers with elevated SGPT, and anti-e in those with normal SGPT. Six carriers whose antigenemia terminated spontaneously had anti-e. The presence of e antigen correlated with a high titer of HBsAg, and with immunofluorescent detection of hepatitis B core antigen in the nuclei of hepatocytes. Conversely, anti-e was associated with significantly lower titers of serum HBsAg (P less than 0.001) and lack of detectable hepatitis B core antigen in the liver.
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PMID:Detection of e antigen and antibody: correlations with hapatitis B surface and hepatitis B core antigens, liver disease, and outcome in hepatitis B infections. 6 Nov 46

Hepatitis B associated antigen (HB-Ag) may be observed in the serum in subjects either apparently healthy or exhibiting a number of disease symptoms. Its incidence among the Geneva voluntary blood donors is 0.48% with 54% exhibiting the surface antigen ad and 34% ay. While the HB-Ag positive blood donors appeared clinically healthy, minor pathology was found in the majority of them (thrombocytopenia, histological evidence of inflammatory foci, of persistent hepatitis and of chronic aggressive hepatitis). In 82 patients suffering from hepatitis B the same ad-ay type distribution of the HB-Ag has been found. In 11 out of 31 patients increased Clq binding suggests the presence of circulating complexes. Diminutions in the level of complement components also indicates participation of complement in the formation of immunocomplexes. In 2 out of 3 patients with Hb-Ag positive polyarteritis nodosa, the Clq binding test was also positive. The pathophysiologic implications of hepatitis B infection are discussed in connection with the authors and other findings. It appears that the main defense mechanism leading to elimination of the viruses within the hepatocytes lies in cell mediated immunity. Hepatitis would then represent the side reaction of this defense mechanism. Antibodies are probably useful in preventing the virus from entering the cell, but also in the course of the cell mediated defense mechanism (elimination of viral material liberated during the T-cell hepatocellular interaction). Immune complexes may be operative in certain extrahepatic manifestations such as arthralgia. Polyarteritis nodosa may result from local antibody interaction with antigen fixed within arterial walls.
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PMID:[Physiopathology of hepatitis B virus infection]. 24 Jan 99

Hepatitis B (surface) antigen (HBSAg) was found in the serum of 8 out of 4 245 women attending the antenatal clinic of the Queen Victoria Maternity Hospital Seven (0, 16%) were asymptomatic carriers of the antigen, while the eigth suffered from polyarteritis nodosa. Seven of the 8 babies born to these mothers were followed-up over periods of up to 18 months, and 1 has become a chronic carrier of HBSAg. The antigen was not detected in the colostrum (breast milk) of the 6 positive mothers tested, but it was present in amniotic fluid, placenta and cord blood of some of the mother-infant couples. The possible routes of transmission of the hepatitis B virus from mother to baby are discussed in the light of these findings. No cases of acute virus B hepatitis occurred in the latter months of pregnancy nor in the puerperium, among 4 088 women delivered at the hospital during this period.
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PMID:Hepatitis B (surface) antigen in mothers and their infants. 24 Feb 7

Recent evidence indicates that viral hepatitis is sometimes associated with the production of extrahepatic tissue injury. Hepatitis B virus (HBV) infection is most commonly incriminated but non-type B hepatitis may also be involved. Three types of syndromes have been recognized. First, a serum sickness-like prodrome consisting of skin eruptions, urticaria and polyarthralgias or arthritis may occur from one to six weeks prior to the onset of hepatitis in 15 to 20 per cent of patients and usually disappears by the time the patient becomes jaundiced. There is extensive evidence that circulating immune complexes are responsible for these symptoms. Second, about 30 to 40 per cent of patients with typical polyarteritis nodosa have persistent hepatitis B surface antigenemia (HBs Ag). Circulating immune complexes composed of HBs Ag, antibody, and complement have been demonstrated together with deposits of immune complexes at sites of vascular injury. Third, an immune complex type of glomerulonephritis may occur following hepatitis B virus infection, usually in association with chronic active hepatitis. Thus there is impressive evidence that hepatitis viruses, especially HBV, may produce a variety of extrahepatic manifestations in which the mechanism of pathogenesis involves an immunologic process rather than direct viral invasion and cytopathogenicity.
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PMID:Extrahepatic manifestations of viral hepatitis. 24 19

The authors have studied the incidence of hepatitis associated antigen (HAA) and the homologous antibody in sera of patients with rheumatoid arthritis on the basis of (1) arthritis sometimes associated with viral hepatitis, (2) the possible infectious etiology of rheumatoid arthritis, and (3) observation on the possible pathogenetic role of HAA in some cases of polyarteritis nodosa. The presence of HAA and antibody titer gave constantly negative results in all subjects examined with the exception of one case which showed no signs of serological or histological hepatic involvement. On the basis of the results obtained, the negligible role of HAA in the etiopathogenesis of rheumatoid arthritis is underlined. However, the authors emphasize as suggestive the hypothesis that the characteristic histopathological alterations of rheumatoid arthritis may be mediated by an immunological reaction toward an infectious agent other than HAA, but operating through mechanisms similar to those of HAA in polyarteritis nodosa.
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PMID:Incidence of hepatitis associated antigen HAA and homologous antibody in patients with rheumatoid arthritis. 111 90

In an attempt to establish the characteristics, circumstances leading to infection and development of polyarteritis nodosa (PN) related to hepatitis B virus (HBV), prognostic factors and outcome, and to define the most effective treatment, 66 patients observed between 1972 and 1989 were analyzed. Hepatitis was clinically present in 19/66 patients before PN. In most cases, PN occurred less than 6 months after infection. Clinical manifestations of PN were comparable to those observed in patients without HBV infection except for orchitis which was present in 13.6% and for pulmonary signs which were absent. Transaminases were normal in 38 cases for SGOT and 31 for SGPT and twice the normal range or more in the other cases. Antineutrophil cytoplasmic antibodies (ANCA) were tested in 22 patients and present in 2 (9%). Twenty-eight patients were treated with prednisone +/- oral cyclophosphamide +/- plasma exchanges. Thirty-eight patients were given a short-term treatment with prednisone followed by the association of vidarabine, 15 mg/kg bw/d for one week and 7.5 mg/kg bw/d for 2 weeks, and plasma exchanges: 14 sessions during the 3 weeks of vidarabine infusion, then tapered until stopping treatment after 2 to 3 months depending upon the clinical results obtained. The mean duration of follow-up was 50.3 +/- 46.1 months. At the end of follow-up, 13 of the 28 patients (46.4%) treated with steroids +/- cyclophosphamide +/- plasma exchanges died and 7/38 (18.4%) of those treated with vidarabine and plasma exchanges (p < 0.001) died. HBe/anti-HBe seroconversion was observed in 2 patients treated with prednisone +/- cyclophosphamide +/- plasma exchanges who were alive at the time of final analysis and in 16 patients receiving the other regimen. The outcome of patients treated with a few days of prednisone, vidarabine and plasma exchange was good and, therefore, we propose this protocol as the first viable treatment for polyarteritis nodosa related to HBV, surpassing the conventional treatment with steroids and cyclophosphamide, which stimulates viral replication.
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PMID:Polyarteritis nodosa related to hepatitis B virus. A retrospective study of 66 patients. 136 69

The authors report the case of a patient with acute alithiasic cholecystitis associated with viral B hepatitis revealing periarteritis nodosa. Histopathological results showed signs of focal arteritis in the gallbladder and liver. Because of the negativity of the viral DNA in serum and the lack of histopathological necrosis in hepatic specimen, the patient was treated by steroid therapy only with a rapid regression of signs of vasculitis and the disappearance of the hepatitis markers.
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PMID:[Alithiasic cholecystitis and viral hepatitis B disclosing periarteritis nodosa]. 197 25


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